[42, 43] Altogether, these data support the idea that even with normal expression of NOS in the corpus cavernosum of db/db mice, the lower levels and activity of the antioxidant enzymes SOD contributes to increase superoxide anion levels, which decreases NO bioavailability, increasing peroxynitrite levels, causing eNOS uncoupling and tissue damage by lipid peroxidation which impairs corpus cavernosum relaxation and lead to erectile dysfunction. The gene discussed is NOS1; the disease is erectile dysfunction.